Owen Samuels

BACKGROUND AND PURPOSE: Atherosclerosis of the major intracranial arteries is an important cause of ischemic stroke. We established measurement criteria to assess percent stenosis of a major intracranial artery (carotid, middle cerebral, vertebral, basilar) and determined the interobserver/intraobserver agreements and interclass/intraclass correlations of these measurements. METHODS: We defined percent stenosis of an intracranial artery as follows: percent stenosis = [(1 - (D(stenosis)/D(normal)))] x 100, where D(stenosis) = the diameter of the artery at the site of the most severe stenosis and D(normal) = the diameter of the proximal normal artery. If the proximal segment was diseased, contingency sites were chosen to measure D(normal): distal artery (second choice), feeding artery (third choice). Using a hand-held digital caliper, three neuroradiologists independently measured D(stenosis) and D(normal) of 24 stenotic intracranial arteries. Each observer repeated the readings 4 weeks later. We determined how frequently two observers' measurements of percent stenosis of each of the 24 diseased arteries differed by 10% or less. RESULTS: Among the three pairs of observers, interobserver agreements were 88% (observer 1 versus observer 2), 79% (observer 1 versus observer 3), 75% (observer 2 versus observer 3) for the first reading and were 75% (observer 1 versus observer 2), 100% (observer 1 versus observer 3), and 71% (observer 2 versus observer 3) for the second reading. Intraobserver agreement for each of the observers was 88%, 83%, and 100%. Interclass correlation was 85% (first reading) and 87% (second reading). Intraclass correlation was 92% (first and second readings combined). CONCLUSION: This method shows good interobserver and intraobserver agreements for the measurement of intracranial stenosis of a major artery. If validated in subsequent studies, this method may serve as a standard for the measurement of percent stenosis of an intracranial artery.

To the Editor: Muscle weakness is a common finding and an important predictor of death in patients with West Nile virus encephalitis. 1,2 Yet this important sign does not have a defined pathological basis.In monkeys, horses, and birds, West Nile virus causes poliomyelitis. [3]4][5] Our clinical and electrodiagnostic findings in three consecutive patients withThe New England Journal of Medicine Downloaded from nejm.org

To evaluate the utility of using magnetic resonance imaging (MRI) of cerebral blood flow (CBF) in conjunction with pharmacologic flow augmentation, the authors imaged 14 patients with ischemic symptoms referable to large artery cerebrovascular stenosis of the anterior circulation. CBF was measured by using continuous arterial spin labeling (CASL) both at rest and 10 minutes after 1 g intravenous acetazolamide on a commercial 1.5 Tesla scanner. Quantitative CBF images were calculated along with augmentation images showing the effects of acetazolamide. Interpretable studies were obtained from all patients. Based on the image data as well as a region of interest analysis of CBF changes in middle cerebral artery distributions, varying patterns of augmentation were observed that suggested differing mechanisms of ischemic symptomatology. The ability to obtain this information in conjunction with a structural MRI examination extends the diagnostic potential for MRI in cerebrovascular disease and allows the value of augmentation testing in clinical management to be assessed more widely. J. Magn. Reson. Imaging 1999;10:870-875.

OBJECTIVE: To describe a patient with transient reversal of findings of brain death after cardiopulmonary arrest and attempted therapeutic hypothermia. DESIGN: Case report. SETTING: Intensive care unit of an academic tertiary care hospital. PATIENT: A 55-yr-old man presented with cardiac arrest preceded by respiratory arrest. Cardiopulmonary resuscitation was performed, spontaneous perfusion restored, and therapeutic hypothermia was attempted for neural protection. After rewarming to 36.5°C, neurologic examination showed no eye opening or response to pain, spontaneous myoclonic movements, sluggishly reactive pupils, absent corneal reflexes, and intact gag and spontaneous respirations. Over 24 hrs, remaining cranial nerve function was lost. The neurologic examination was consistent with brain death. Apnea test and repeat clinical examination after a duration of 6 hrs confirmed brain death. Death was pronounced and the family consented to organ donation. Twenty-four hrs after brain death pronouncement, on arrival to the operating room for organ procurement, the patient was found to have regained corneal reflexes, cough reflex, and spontaneous respirations. The care team faced the challenge of offering an adequate explanation to the patient's family and other healthcare professionals involved. INTERVENTIONS: Induced hypothermia and brain death determination. MEASUREMENTS AND MAIN RESULTS: This represents the first published report in an adult patient of reversal of a diagnosis of brain death made in full adherence to American Academy of Neurology guidelines. Although the reversal was transient and did not impact the patient's prognosis, it impacted his eligibility for organ donation and cast doubt about the ability to determine irreversibility of brain death findings in patients treated with hypothermia after cardiac arrest. CONCLUSIONS: We strongly recommend caution in the determination of brain death after cardiac arrest when induced hypothermia is used. Confirmatory testing should be considered and a minimum observation period after rewarming before brain death testing ensues should be established.